Arteriosclerosis, Thrombosis, and Vascular Biology. 1999;19:546-551
© 1999 American Heart Association, Inc.
Original Contributions |
PPAR
Activation in Human Endothelial Cells Increases Plasminogen Activator Inhibitor Type-1 Expression
PPAR as a Potential Mediator in Vascular Disease
From the Vascular Medicine and Atherosclerosis Unit, Cardiovascular Division, Brigham and Women's Hospital, Harvard Medical School, Boston, Mass.
Correspondence to Jorge Plutzky, MD, Vascular Medicine and Atherosclerosis Unit, Cardiovascular Division, Brigham and Women's Hospital, Harvard Medical School, 221 Longwood Ave, Boston, MA 02115. E-mail JPlutzky{at}BICS.BWH.HARVARD.EDU
Abstract—Plasminogen
activator inhibitor type-1 (PAI-1) is a major
physiological inhibitor of
fibrinolysis, with its plasma levels correlating with
the risk for myocardial infarction and venous thrombosis. The
regulation of PAI-1 transcription by endothelial cells
(ECs), a major source of PAI-1, remains incompletely understood.
Adipocytes also produce PAI-1, suggesting possible common regulatory
pathways between adipocytes and ECs. Peroxisomal
proliferator-activated receptor-
(PPAR) is a
ligand-activated transcription factor that regulates gene
expression in response to various mediators such as
15-deoxy-
12,14-prostaglandin J2
(15d-PGJ2) and oxidized linoleic acid (9- and 13-HODE). The
present study tested the hypotheses that human ECs express PPAR
and that this transcriptional activator regulates PAI-1
expression in this cell type. We found that human ECs contain both
PPAR mRNA and protein. Immunohistochemistry of human carotid
arteries also revealed the presence of PPAR in ECs. Bovine ECs
transfected with a PPAR response element (PPRE)–luciferase construct
responded to stimulation by the PPAR agonist 15d-PGJ2 in
a concentration-dependent manner, suggesting a functional PPAR in
ECs. Treatment of human ECs with 15d-PGJ2,
9(S)-HODE, or 13(S)-HODE augmented PAI-1
mRNA and protein expression, whereas multiple PPAR
activators did not change PAI-1 levels. Introduction of
increasing amounts of a PPAR expression construct in human
fibroblasts enhanced PAI-1 secretion from these cells in proportion to
the amount of transfected DNA. Thus, ECs express functionally active
PPAR that regulates PAI-1 expression in ECs. Our results establish a
role for PPAR in the regulation of EC gene expression, with
important implications for the clinical links between obesity and
atherosclerosis.
Key Words: atherosclerosis • endothelium • peroxisomal proliferator-activated receptor • plasminogen activator inhibitor-1 • 15-deoxy-12,14-prostaglandin J2
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I. Brocheriou, D. Stengel, L. Mattsson-Hulten, J. Stankova, M. Rola-Pleszczynski, F. Koskas, O. Wiklund, Y. Le Charpentier, and E. Ninio Expression of Platelet-Activating Factor Receptor in Human Carotid Atherosclerotic Plaques : Relevance to Progression of Atherosclerosis Circulation, November 21, 2000; 102(21): 2569 - 2575. [Abstract] [Full Text] [PDF]
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 T. Murata, S. He, M. Hangai, T. Ishibashi, X.-P. Xi, S. Kim, W. A. Hsueh, S. J. Ryan, R. E. Law, and D. R. Hinton Peroxisome Proliferator-Activated Receptor-{gamma} Ligands Inhibit Choroidal Neovascularization Invest. Ophthalmol. Vis. Sci., July 1, 2000; 41(8): 2309 - 2317. [Abstract] [Full Text]
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N. Marx, F. Mach, A. Sauty, J. H. Leung, M. N. Sarafi, R. M. Ransohoff, P. Libby, J. Plutzky, and A. D. Luster Peroxisome Proliferator-Activated Receptor-{gamma} Activators Inhibit IFN-{gamma}-Induced Expression of the T Cell-Active CXC Chemokines IP-10, Mig, and I-TAC in Human Endothelial Cells J. Immunol., June 15, 2000; 164(12): 6503 - 6508. [Abstract] [Full Text] [PDF]
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G. Chinetti, F. G. Gbaguidi, S. Griglio, Z. Mallat, M. Antonucci, P. Poulain, J. Chapman, J.-C. Fruchart, A. Tedgui, J. Najib-Fruchart, et al. CLA-1/SR-BI Is Expressed in Atherosclerotic Lesion Macrophages and Regulated by Activators of Peroxisome Proliferator-Activated Receptors Circulation, May 23, 2000; 101(20): 2411 - 2417. [Abstract] [Full Text] [PDF]
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V. Pasceri, H. D. Wu, J. T. Willerson, and E. T. H. Yeh Modulation of Vascular Inflammation In Vitro and In Vivo by Peroxisome Proliferator-Activated Receptor-{gamma} Activators Circulation, January 25, 2000; 101(3): 235 - 238. [Abstract] [Full Text] [PDF]
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 B. Desvergne and W. Wahli Peroxisome Proliferator-Activated Receptors: Nuclear Control of Metabolism Endocr. Rev., October 1, 1999; 20(5): 649 - 688. [Abstract] [Full Text]
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P. Delerive, F. Martin-Nizard, G. Chinetti, F. Trottein, J.-C. Fruchart, J. Najib, P. Duriez, and B. Staels Peroxisome Proliferator-Activated Receptor Activators Inhibit Thrombin-Induced Endothelin-1 Production in Human Vascular Endothelial Cells by Inhibiting the Activator Protein-1 Signaling Pathway Circ. Res., September 3, 1999; 85(5): 394 - 402. [Abstract] [Full Text] [PDF]
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N. Marx, G. K. Sukhova, T. Collins, P. Libby, and J. Plutzky PPAR{alpha} Activators Inhibit Cytokine-Induced Vascular Cell Adhesion Molecule-1 Expression in Human Endothelial Cells Circulation, June 22, 1999; 99(24): 3125 - 3131. [Abstract] [Full Text] [PDF]
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P. Delerive, P. Gervois, J.-C. Fruchart, and B. Staels Induction of Ikappa Balpha Expression as a Mechanism Contributing to the Anti-inflammatory Activities of Peroxisome Proliferator-activated Receptor-alpha Activators J. Biol. Chem., November 17, 2000; 275(47): 36703 - 36707. [Abstract] [Full Text] [PDF]
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M. Fu, X. Zhu, Q. Wang, J. Zhang, Q. Song, H. Zheng, W. Ogawa, J. Du, and Y. E. Chen Platelet-Derived Growth Factor Promotes the Expression of Peroxisome Proliferator-Activated Receptor {gamma} in Vascular Smooth Muscle Cells by a Phosphatidylinositol 3-Kinase/Akt Signaling Pathway Circ. Res., November 23, 2001; 89(11): 1058 - 1064. [Abstract] [Full Text] [PDF]
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N. Marx, B. Kehrle, K. Kohlhammer, M. Grub, W. Koenig, V. Hombach, P. Libby, and J. Plutzky PPAR Activators as Antiinflammatory Mediators in Human T Lymphocytes: Implications for Atherosclerosis and Transplantation-Associated Arteriosclerosis Circ. Res., April 5, 2002; 90(6): 703 - 710. [Abstract] [Full Text] [PDF]
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